ライフサイエンスコーパス: pericyte

1 ibrotic scar would depend on dividing NG2(+) pericytes.

2 7 transcription factor in PDGF-BB-stimulated pericytes.

3 gulate BBB functions in HIV infection of BBB pericytes.

4 eta-cell dedifferentiation in the absence of pericytes.

5 t allows diphtheria toxin-based depletion of pericytes.

6 markers characteristic of neuronal cells and pericytes.

7 ls expressed surface markers associated with pericytes.

8 architecture but was normal in mice lacking pericytes.

9 which transfer miR-503 from ECs to vascular pericytes.

10 essential factor for maintaining GSC-derived pericytes.

11 nd limited the loss of endothelial cells and pericytes.

12 cyclase activation that probably occurred in pericytes.

13 pressed by tumour-associated fibroblasts and pericytes.

14 ted to capillary constriction by contractile pericytes.

15 (EB) dye, and loss of endothelial cells and pericytes 1 day after SCI compared to non-diabetic rats.

16 pes (Pldv and Elu) and a small percentage of pericytes (2.5%) comprised 44% and 51% of the new NG2(+)

17 (PDGFRbeta) is highly expressed in activated pericytes, a main source of fibroblasts.

18 Pericyte ablation also led to hypoxic focal and subclini

19 Ten days after pericyte ablation, we observed endothelial cell damage b

20 Here, we have shown that pericytes activate a TLR2/4- and MyD88-dependent proinfl

21 Similarly to classic immune cells, pericytes activate the NLRP3 inflammasome, leading to IL

22 Pericytes adhere to the abluminal surface of endothelial

23 l vascular leak, possibly through effects on pericyte adhesion and migration, and reveal alphavbeta5

24 Pericytes, along with endothelial cells, make up the den

25 In conclusion, pericyte alpha-SMA phenotype mediates acute microvessel

26 We found modulating eNOS regulated pericyte alpha-SMA phenotype transformation, microcircul

27 Therefore, by targeting the eNOS and pericyte alpha-SMA phenotype, our present data may shed

28 nd antiapoptotic actions through endothelial-pericyte and endothelial-cardiomyocyte crosstalk in the

29 ctivity of the p75(NTR) receptor can promote pericyte and vascular dysfunction, inflammation, glial a

30 ne local regulation of capillary diameter by pericytes and a role for gap junctions in vascular netwo

31 lls phenotypically and functionally resemble pericytes and are indispensable for vascular stabilizati

32 croscopy to examine the relationship between pericytes and blood plasma leakage during photothromboti

33 n inducing alpha-SMA expressions in cultured pericytes and brain slices via inhibiting NO/cGMP pathwa

34 expression was significantly elevated in PAH pericytes and correlated with reduced mitochondrial meta

35 th ibrutinib selectively targeted neoplastic pericytes and disrupted the BTB, but not the BBB, thereb

36 observed increased distance between Gli1(+) pericytes and endothelial cells after AKI (mean+/-SEM: 3

37 c inducible overexpression of CTGF by kidney pericytes and fibroblasts had no bearing on nephrogenesi

38 We show that proliferating NG2(+) pericytes and glia largely segregate into the fibrotic a

39 ese data reveal that acutely dividing NG2(+) pericytes and glia play fundamental roles in post-SCI ti

40 ted capillary endothelial cells covered with pericytes and glia, but the role of the pericytes in BRB

41 owever, two NG2-expressing cell populations, pericytes and glia, may also influence scar formation.

42 plicate an association between a decrease of pericytes and liver disease caused by ligature-induced p

43 Within this tumor stroma, vessel-associated pericytes and myofibroblasts share a number of traits, i

44 nged anatomically adjacent to blood vessels, pericytes and nerves, suggesting an astrocyte-like pheno

45 Interactions between pericytes and neutrophils in culture yielded even higher

46 ricytes, we asked whether cross-talk between pericytes and NSCs was induced by CORM-3, thereby promot

47 cells distributed throughout the BM, and on pericytes and perivascular cells in multiple organs.

48 e-resident PDGFRbeta(+) cells, which include pericytes and PW1(+) interstitial cells (PICs), play a d

49 Far from being passive and quiescent, pericytes and resident fibroblasts are busily sensing an

50 Pericytes and smooth muscle cells are integral component

51 easing age, mutated Notch3 aggregated around pericytes and smooth muscle cells.

52 und that pre-seeded ASCs differentiated into pericytes and stabilized the endothelial cell (EC) monol

53 ion between human donor control and PAH lung pericytes and the link between mitochondrial dysfunction

54 However, the origin of CNS microvascular pericytes and the mechanism of their recruitment remain

55 Many functional properties of pericytes and their exact role in the regulation of angi

56 e examine the key signaling pathways between pericytes and their neighboring endothelial cells, astro

57 We found that density of pericytes and their sensitivity to stimulation were redu

58 urvival, but for sustained interactions with pericytes and vascular smooth muscle cells (VSMCs) regul

59 transcription factor Tbx18 selectively marks pericytes and vascular smooth muscle cells in multiple o

60 n inducible Tbx18-CreERT2 line revealed that pericytes and vascular smooth muscle cells maintained th

61 Loss of mural cells, which encompass pericytes and vascular smooth muscle cells, is a hallmar

62 nit (NVU) that includes neurons, astrocytes, pericytes, and microglia as well as the blood vessels th

63 ganglioside is stored in microglia, vascular pericytes, and neurons, causing micro- and astrogliosis,

64 n endothelial cells, astrocytes, neurons and pericytes, and therefore are often consuming and technic

65 ens junction protein between endothelium and pericytes; and increases in the vessel destabilizing age

66 Transplantation of adventitial pericytes (APCs) improves recovery from tissue ischemia

67 totic complex can block high glucose-induced pericyte apoptosis, widely considered a hallmark feature

68 SIGNIFICANCE STATEMENT: Pericytes are a key component of the neurovascular unit

69 We demonstrate that capillary pericytes are a population of mural cells with distinct

70 Pericytes are believed to originate from either mesenchy

71 While pericytes are builders and custodians of the BBB in the

72 However, during acute ischemia, we find that pericytes are involved in creating rapid and heterogeneo

73 lial cells, the endothelium, and surrounding pericytes are key players in the progression to chronic

74 Pericytes are perivascular mural cells of brain capillar

75 To conclude, our findings suggest that pericytes are pivotal components of the islet niche, whi

76 rst time, our data show that dividing NG2(+) pericytes are required for post-SCI angiogenesis, which

77 Cardiac pericytes are therefore a novel therapeutic target in is

78 CNS pericytes are uniquely positioned in the neurovascular u

79 Pericytes are vascular mural cells embedded in the basem

80 Pericytes are widely believed to function as mesenchymal

81 ing vascular smooth muscle cells (vSMCs) and pericytes, are involved in new vessel formation and in p

82 -negative endothelial cells and SMA-positive pericytes arranged in macro- or microlobules.

83 lts challenge the current view of endogenous pericytes as multipotent tissue-resident progenitors and

84 Abnormalities of islet pericytes, as implicated in type 2 diabetes, may therefo

85 We show that Nestin(+)NG2(+) pericytes associate with portal vessels, forming a niche

86 ontaneous EMT, a substantial fraction of the pericytes associated with tumor vasculature were derived

87 hibitor, but not an MMP-2 inhibitor, reduced pericyte-associated FITC-gelatin fluorescence and plasma

88 Pericytes at the corticomedullary junction produce the S

89 clusion-induced ocular ischemia, we observed pericytes (at d 2, using Gd-nestin, by eyedrop solution)

90 These findings suggest that EMT confers key pericyte attributes on cancer cells.

91 e model of oxygen-induced retinopathy (OIR), pericytes become the predominant CCN1 producing cells.

92 ant gene candidates associated with aberrant pericyte behavior, we performed a transcriptome analysis

93 the expression of the non-canonical Wnt5a in pericyte but not in EC cultures.

94 th factor, enhanced ASC differentiation into pericytes but overstimulated their proliferation, causin

95 tion and wound healing responses in cultured pericytes, but domain 4 showed the broadest profibrotic

96 expressed in cultured MSCs, fibroblasts and pericytes, but not other types of cells including epithe

97 Moreover, loss of cycling NG2(+) glia and pericytes caused significant multicellular tissue change

98 yrosine kinase receptor that is required for pericyte cell survival; N-cadherin, the key adherens jun

99 onical Wnt signaling pathway in interstitial pericytes cell autonomously drives myofibroblast activat

100 ghlight the significance of CCN1-EC and CCN1-pericyte communication signals in driving physiological

101 exposed to laminar flow and cocultured with pericytes confirmed that atrasentan reduced endothelial

102 Thus, cardiac pericytes constrict coronary capillaries and reduce micr

103 The mechanism by which pericytes contribute to BBB damage warrants further inve

104 These results suggest that pericytes contribute to rapid and localized proteolytic

105 nsisting of vascular smooth muscle cells and pericytes cover the endothelial cells (ECs) to regulate

106 scue of the endothelial gene tight junction, pericyte coverage and extracellular-matrix deficits.

107 ssels in Apoa1bp(-/-) mice manifested normal pericyte coverage and vascular integrity.

108 or vasculature revealed a strong increase of pericyte coverage and vessel perfusion both in mPDAC and

109 s, diminished AQP4 expression, and decreased pericyte coverage are responsible for the BBB disruption

110 Inhibition of VEGF signalling increases pericyte coverage in microvessels.

111 We found that pericyte coverage of tumor vasculature is inversely corr

112 scopy and polymer casts that show incomplete pericyte coverage of tumour vessels and the presence of

113 ascular density, vessel diameter and reduced pericyte coverage resulting in enhanced tumor growth in

114 laries per high power field (c/hpf) and NG2+ pericyte coverage were analyzed.

115 us VEGF signalling prevents excess neovessel pericyte coverage, and is required for VSMC recruitment

116 EMT cells in transplanted tumors diminished pericyte coverage, impaired vascular integrity, and atte

117 ssel normalization, which involves increased pericyte coverage, improved tumour vessel perfusion, red

118 uding tortuous retinal vessels and defective pericyte coverage.

119 pillary density, number of CD31(+) cells and pericyte coverage.

120 ular diameter or flow changes in SMC but not pericyte-covered microvessels.

121 In pericyte cultures that were undergoing oxygen and glucos

122 hat these autoantibodies could contribute to pericyte damage through complement activation.

123 with CO-releasing molecule (CORM)-3 reduced pericyte death and ameliorated the progression of neurol

124 Retinal pericyte death is an early pathologic feature of DR.

125 ert-butyl-a-phenylnitrone (PBN) also reduced pericyte death, neurological outcomes were not rescued.

126 a therapeutic approach for TBI by preventing pericyte death, rescuing cross-talk with NSCs and promot

127 Occludin in BBB pericytes decreased by 10% during the first 48 h after H

128 Using loss-of-function pericyte-deficient mice, here we show that pericyte dege

129 Thus, pericyte degeneration as seen in neurological disorders

130 n pericyte-deficient mice, here we show that pericyte degeneration diminishes global and individual c

131 e 1 mice showed GC loss but no difference in pericyte density or acellular capillaries.

132 imensional microfluidics system identified a pericyte-dependent role for alphavbeta5 in modulating va

133 weak inducer of apoptosis (TWEAK), promoted pericyte-dependent vasoconstriction followed by pericyte

134 Angiogenic defects caused by pericyte depletion are phenocopied by intraocular inject

135 ta indicate that a subset of cerebrovascular pericytes derive from mature macrophages in the very ear

136 Here, we investigate the function of pericyte-derived laminin in vascular integrity.

137 Together, these data suggest that pericyte-derived laminin is involved in the maintenance

138 s activity of monoamine receptors (5-HT1) on pericytes, despite the absence of monoamines.

139 sis provides direct evidence that AKI causes pericyte detachment from capillaries, and that pericyte

140 icyte-dependent vasoconstriction followed by pericyte detachment from capillaries.

141 ere, we show a new source of cerebrovascular pericytes during neurogenesis.

142 on which resulted in a dramatic reduction of pericyte/EC coverage and exacerbation of LPS-induced vas

143 eased HIF-2alpha/Notch3 expression, improved pericyte/EC coverage and reduced the mortality rate in t

144 ibited Ang-1/Tie-2 expression with a reduced pericyte/EC coverage.

145 ure of invading endothelial cells to recruit pericytes efficiently, whereas deletion later in embryog

146 nsists of endothelial cells, astrocytes, and pericytes embedded in basal lamina (BL).

147 strocytes, while brain endothelial cells and pericytes encase the surface, acting as a barrier that r

148 dherin and VE-cadherin, thereby compromising pericyte-endothelial cell interactions and inter-endothe

149 HIF-2alpha, Notch3 and angiopoietins/Tie-2, pericyte/endothelial (EC) coverage and vascular permeabi

150 y formed vessels (from 27 +/- 2 to 54 +/- 3% pericyte ensheathment).

151 /PDGFRbeta/desmin-expressing cerebrovascular pericytes, enwrapping and associating with vascular endo

152 selectively inactivated in their pancreatic pericytes exhibited impaired glucose tolerance due to co

153 f patient-derived donor control and PAH lung pericytes followed by functional genomics analysis.

154 n cells in their microenvironment, including pericytes, for their proper function.

155 identified functions that discriminate lung pericytes from resident fibroblasts, identified a subset

156 cal and anatomical evidence that both intact pericyte function as well as gap junction-mediated signa

157 branches and the enlargement of vessels when pericyte function is impaired or lost.

158 t-fed mice had greater atrophic capillaries, pericyte ghosts, and permeability than controls.

159 l/glial antigen 2 (NG2) expressed in hepatic pericytes, glutathione (GSH), and malondialdehyde (MDA)

160 Compared with donor control cells, PAH pericytes had significant enrichment of genes involved i

161 ble specificity for dye uptake suggests that pericytes have molecular transport mechanisms not presen

162 sults indicate that islets depleted of their pericytes have reduced insulin content and expression.

163 lts from this study demonstrate that MSC and pericytes have significant bone regeneration potential i

164 d that increased PDK4 is associated with PAH pericyte hyperproliferation and reduced endothelial-peri

165 vessel growth requires proliferating NG2(+) pericytes; if this were also true in the CNS, then the f

166 We demonstrate feasibility of longitudinal pericyte imaging during microvascular development and ag

167 in endothelial cells and the contribution of pericytes, immune cells, and matrix metalloproteinases.

168 em cells (MSC) as a potential substitute for pericytes in a BBB model.

169 that MSC contributed in a similar manner to pericytes in a co-cultured 3D model on increasing trans-

170 The ability to easily label pericytes in any mouse model opens the possibility of a

171 with pericytes and glia, but the role of the pericytes in BRB regulation is not fully understood.

172 We also review the role of pericytes in CNS disorders including rare monogenic dise

173 urs at the interface between endothelium and pericytes in human pancreatic cancer.

174 Ex vivo depletion of pericytes in isolated islets resulted in a similar impai

175 role for endosialin-expressing primary tumor pericytes in mediating metastatic dissemination and iden

176 ial cells, human astrocytes, and human brain pericytes in mono-, co-, and tricultures.

177 glial antigen 2, a known molecular marker of pericytes in multiple organs.

178 ze EPO may represent a functional feature of pericytes in the brain and kidney.

179 r studies provide experimental evidence that pericytes in the brain have the ability to function as o

180 We found that pericytes in the brain synthesized EPO in mice with gene

181 lts reveal that loss of proliferating NG2(+) pericytes in the lesion prevented intralesion angiogenes

182 e directly tested the role of Gli1(+) kidney pericytes in the maintenance of peritubular capillary he

183 of distinct populations of neurons, glia and pericytes in the mouse brain and in zebrafish.

184 is accompanied by a marked reduction in NG2+ pericytes in the periodontitis group compared with the c

185 Mechanistically, endosialin-expressing pericytes in the primary tumor facilitate distant site m

186 The role of pericytes in the regulation of cerebral blood flow (CBF)

187 n preserving vascular integrity by targeting pericytes in the setting of LPS-induced sepsis.

188 ions in the adhesion and migration of kidney pericytes in vitro Initial studies monitoring renal bloo

189 ever, the cell fate plasticity of endogenous pericytes in vivo remains unclear.

190 Eliminating GSC-derived pericytes in xenograft models disrupted BTB tight juncti

191 Lack of differentiated pericytes initiates a scenario of structural and functio

192 l therapeutic targets to improve endothelial-pericyte interactions and prevent small vessel loss in P

193 Defective endothelial cell-pericyte interactions are frequently observed in disease

194 Reduced endothelial-pericyte interactions are linked to progressive small ve

195 Cathepsin D plays a role in endothelial-pericyte interactions during alteration of the blood-ret

196 ondrial dysfunction and aberrant endothelial-pericyte interactions in PAH.

197 dase-4 (DPP4) inhibitor on CD in endothelial-pericyte interactions in vitro and in vivo.

198 lso examined the effect of CD on endothelial-pericyte interactions, as well as the effect of dipeptid

199 cell proliferation, and improved endothelial-pericyte interactions.

200 e hyperproliferation and reduced endothelial-pericyte interactions.

201 ration of TWEAK activated and differentiated pericytes into cytokine-producing myofibroblasts, and fu

202 The mechanism of IL6 action on pericytes involved stimulation of the Notch ligand Jagge

203 , we show that Tcf7l2 activity in pancreatic pericytes is required for beta-cell function.

204 Cultured pericytes isolated from distinct tissues can differentia

205 Additionally, pericytes isolated from these mice became hypermigratory

206 We imaged pericyte-labeled transgenic mice with in vivo two-photon

207 ll lines with either osteogenic potential or pericyte-like angiogenic function.

208 etween peritubular capillary endothelium and pericyte-like fibroblasts, leading to myofibroblast tran

209 Moreover, PC-M cells had pericyte-like functionality being capable of co-localizi

210 cells potently inhibits the formation of the pericyte-like scaffold, with concomitant attenuation of

211 , that is, the spreading of tumor cells in a pericyte location along abluminal vascular surfaces.

212 g a genetic ablation model, we asked whether pericyte loss alone is sufficient for capillary destabil

213 drolase (sEH) as a key enzyme that initiates pericyte loss and breakdown of endothelial barrier funct

214 ated the involvement of SIRT3 in LPS-induced pericyte loss and microvascular dysfunction.

215 ssion of Sirt3 further prevented LPS-induced pericyte loss and vascular leakage.

216 with a specific sEH inhibitor prevented the pericyte loss and vascular permeability that are charact

217 explants revealed capillary rarefaction and pericyte loss compared to nondiabetic explants.

218 ar capillary health, and the consequences of pericyte loss during injury.

219 Recent studies reveal a crucial role of pericyte loss in sepsis-associated microvascular dysfunc

220 Although selective pericyte loss in stable adult retinal vessels surprising

221 ricyte detachment from capillaries, and that pericyte loss is sufficient to trigger transient tubular

222 Furthermore, pericyte loss led to significantly reduced capillary num

223 tures including basement membrane reduction, pericyte loss, and astrocyte dysfunction.

224 a cirrhotic liver, and co-localized with the pericyte marker (immunohistochemistry: PDGFR-beta) and C

225 Both MSC and pericyte markers in 2D culture environment were evaluate

226 EMT markedly activated multiple pericyte markers in carcinoma cells, in particular PDGFR

227 lose the expression of traditional vSMC and pericyte markers in response to tumor-secreted factors a

228 Because pericytes mediate important functions in the CNS, includ

229 We show that p75NTR in glia and in pericytes mediate ligand-dependent induction of inflamma

230 isruption of this MyD88-dependent pathway in pericytes might be a potential therapeutic approach to i

231 effector kinase IRAK4 intrinsically control pericyte migration and conversion to myofibroblasts.

232 ls enhance macrophage migration but restrain pericyte mobilisation.

233 s suggest that apoE has an intrinsic role in pericyte mobility, which is vital in maintaining cerebro

234 e investigated the potential role of apoE in pericyte mobility.

235 E-cadherin endocytosis in ECs, and rendering pericytes more quiescent and adhesive (via upregulation

236 impacts on functional properties of muscular pericytes (MPs), which are resident stem cells committed

237 Released IL-1beta signals through pericyte MyD88 to amplify this response.

238 Our data show that in pericytes, MyD88 and IRAK4 are key regulators of 2 major

239 These data indicate that pericyte-neutrophil interactions play a role in mediatin

240 y compares phenotype characteristics between pericytes, obtained from human adipose tissue, different

241 uration of BRB through active recruitment of pericytes onto growing retinal vessels.

242 Specific ablation of MyD88 in pericytes or pharmacological inhibition of MyD88 signali

243 Pericytes (PCs) are endothelium-associated cells that pl

244 ed microvascular endothelial cells (ECs) and pericytes (PCs) that form the wall of the postcapillary

245 and possible mechanism of hemoglobin induced pericyte phenotype transformation in the regulation of m

246 Pericytes play a critical role in the cerebrovasculature

247 It has recently been reported that pericytes play important roles in the central nervous sy

248 ural cells (vascular smooth muscle cells and pericytes) play an essential role in the development of

249 ith increased numbers at the abluminal face, pericyte process detachment and disruption of the periva

250 and uniform basement membrane surrounded by pericyte processes.

251 To conclude, we suggest that pancreatic pericytes produce secreted factors, including BMP4, in a

252 n nondiabetic retina, focal stimulation of a pericyte produced a robust vasomotor response, which pro

253 Here we show that pericytes promote endothelial sprouting in the postnatal

254 Our findings establish that pericytes promote endothelial sprouting, which results i

255 gh stimulating angiogenesis, induced neither pericyte recruitment nor collateral growth.

256 ent (both 0%), and VEGF inhibition increased pericyte recruitment to newly formed vessels (from 27 +/

257 Impaired pericyte recruitment to the vessels shows multiple vascu

258 The pericyte relaxant adenosine increased capillary diameter

259 is has been vastly investigated, the role of pericytes remains largely unknown.

260 situ hybridization, we determined that brain pericytes represent an important cellular source of Epo

261 Pericytes represent important support cells surrounding

262 Pericytes, resident fibroblasts, and mesenchymal stem ce

263 The loss of retinal pericytes (RPCs) is a hallmark of early stage diabetic r

264 icantly reduced the microvessel diameters at pericyte sites, due to the effects of hemoglobin inducin

265 ce yielded microvessels that were covered by pericytes, smooth muscle cells, and a collagen-fortified

266 ree times greater frequency in regions where pericyte somata adjoined the endothelium.

267 Pericyte somata covered only 7% of the total capillary l

268 osine increased capillary diameter by 21% at pericyte somata, decreased capillary block by 25% and in

269 ivation of matrix metalloproteinase (MMP) at pericyte somata, which was visualized at high resolution

270 thelial growth factor receptor 1 (VEGFR1) by pericytes spatially restricts VEGF signalling.

271 Pericyte-specific deletion of CCN1 significantly decreas

272 copied by intraocular injection of VEGF-A or pericyte-specific inactivation of the murine gene encodi

273 We used perivascular-cell-specific and pericyte-specific lineage-tracing models to trace the fa

274 hat targeting glioma stem cell (GSC)-derived pericytes specifically disrupts the BTB and enhances dru

275 it, brain endothelial cells, astrocytes, and pericytes synthesize and deposit different laminin isofo

276 tion of trace amines (such as tryptamine) by pericytes that ectopically express the enzyme aromatic L

277 stem cells (MSC), and human adipose derived pericytes (the native ancestor of the MSC) delivered per

278 ological and immunohistochemical analyses of pericytes, the capillary vasomotor elements.

279 Pericytes, the precursors of myofibroblasts, are a sourc

280 hylation and repression of erythropoietin in pericytes; these effects were prevented by 5-azacytidine

281 Here, we focus on contribution of pericytes to beta-cell function.

282 ely control the metabolic responses of human pericytes to HIV.

283 This monoamine-receptor activity causes pericytes to locally constrict capillaries, which reduce

284 TR) is upregulated very early in glia and in pericytes to mediate ligand-dependent induction of infla

285 e clinical potential of targeting neoplastic pericytes to significantly improve treatment of brain tu

286 r levels of type II collagen were noted when pericytes undergo chondrogenesis in the hydrogel in the

287 oma cancer cells (344SQ) and endothelial and pericyte vascular cells encapsulated in cell-adhesive, p

288 Stages of progression comprise pericyte/vascular dysfunction, inflammation, glial activ

289 ation between vascular endothelial cells and pericytes/vSMCs.

290 e determined that Epo transcription in brain pericytes was HIF-2 dependent and cocontrolled by PHD2 a

291 ause NSCs seemed to be in close proximity to pericytes, we asked whether cross-talk between pericytes

292 esize EPO is a general functional feature of pericytes, we used conditional gene targeting to examine

293 ion SAH rat model, brain slices and cultured pericytes were used, and intervened with endothelial nit

294 apillary blockages colocalised strongly with pericytes, where capillary diameter was reduced by 37%.

295 oblast-like FOXD1+ progenitor-derived kidney pericytes, which are characterized by the expression of

296 In mice, renal injury-induced activation of pericytes, which are myofibroblast precursors attached t

297 t protein kinase II in endothelial cells and pericytes, which disrupts adherens junction structure an

298 nt Nissl dye NeuroTrace 500/525 labels brain pericytes with specificity, allowing high-resolution opt

299 Co-activation of pericytes with TNF-alpha and IL-17A also elevated fibron

300 Prolonged dual activation of cultured human pericytes with TNF-alpha and IL-17A augmented collagen I